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Understanding the pathogenesis of T1D should facilitate the development of novel disease biomarkers and therapeutics that can accomplish a stated goal of NIDDK, to block T1D progression before complete cell destruction. The major emphasis placed on disease associated genetic mutations or polymorphisms to understand the genetics of T1D has failed to advance either understanding of T1D pathogenesis or to identify therapeutic targets. Recent studies from the Fathman lab have demonstrated that tissue- and disease-specific changes in mRNA expression, rather than DNA variants, may underlie the progression of T1D. Work to be presented emphasizes the importance of studying the control of tissue-specific gene expression in relationship to the pathogenesis of T1D. By combining their expertise in T1D research with their established preclinical models and patient samples/tissues from their collaborator, the Network for Pancreatic Organ Donors with Diabetes, nPOD http://www.jdrfnpod.org, Fathman and colleagues have both demonstrated a potential defect in peripheral tolerance in NOD mice that has homologies in T1D patients and have demonstrated that appropriate immunotherapy may overcome this defect
The NIH Wednesday Afternoon Lecture Series includes weekly scientific talks by some of the top researchers in the biomedical sciences worldwide.
